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Review
. 2017:2017:2608605.
doi: 10.1155/2017/2608605. Epub 2017 Jan 3.

The Histone Modification Code in the Pathogenesis of Autoimmune Diseases

Yasuto Araki  1 , Toshihide Mimura  1
Affiliations
Review

The Histone Modification Code in the Pathogenesis of Autoimmune Diseases

Yasuto Araki et al. Mediators Inflamm. 2017.

Abstract

Autoimmune diseases are chronic inflammatory disorders caused by a loss of self-tolerance, which is characterized by the appearance of autoantibodies and/or autoreactive lymphocytes and the impaired suppressive function of regulatory T cells. The pathogenesis of autoimmune diseases is extremely complex and remains largely unknown. Recent advances indicate that environmental factors trigger autoimmune diseases in genetically predisposed individuals. In addition, accumulating results have indicated a potential role of epigenetic mechanisms, such as histone modifications, in the development of autoimmune diseases. Histone modifications regulate the chromatin states and gene transcription without any change in the DNA sequence, possibly resulting in phenotype alteration in several different cell types. In this paper, we discuss the significant roles of histone modifications involved in the pathogenesis of autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, primary biliary cirrhosis, and type 1 diabetes.

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Conflict of interest statement

The authors have no conflicting financial interests.

Figures

Figure 1
Figure 1
In genetically predisposed individuals, several environmental factors, along with aberrant epigenetic mechanisms, induce a loss of immunological self-tolerance, resulting in the development of autoimmune diseases.
Figure 2
Figure 2
(a) Histone modifications, including methylation, acetylation, ubiquitination, phosphorylation, and sumoylation, have various biological functions, such as the regulation of chromatin states and gene transcription. (b) Lysine residues of histone tails are subject to monomethylation (me1), dimethylation (me2), or trimethylation (me3). (c) Arginine residues of histone tails are subject to monomethylation (me1), symmetrical dimethylation (me2s), or asymmetrical dimethylation (me2a).
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